Vitamin B6 deficiency in maintenance dialysis patients: metabolic effects of repletion

Abstract
Vitamin B6 deficiency is often present in uremic patients, particularly those undergoing dialysis. The contribution of this deficiency to abnormal amino acid and lipid metabolism and to depressed immune function in maintenance dialysis patients was studied. EGOT activity and EGOT indices (i.e., the ratio of activity of EGOT stimulated with exogenous pyridoxal-5′-phosphate to EGOT activity alone) were measured in 15 dialysis patients (D) ingesting at least 2 mg pyridoxine HCl/day and in nine controls (C). EGOT activity was lower (389 ± 18 U/liter) in D as compared to (534 ± 41 U/liter) in C (P < 0.01). EGOT indices in D (1.68 ± 0.07) and C (1.59 ± 0.08) did not differ significantly. After 14 days of 300 mg/day pyridoxine HCl (B6) oral supplementation, EGOT activity increased to a similar range in D (800 ± 47 U/liter) and C (867 ± 43 U/liter). Immune responsiveness as assessed by spontaneous reactive lymphocyte blastogenesis and lymphocyte reactivity to Con A and phytohemagglutinin was within the normal range in D before and after B6. Serum high-density lipoprotein levels increased significantly in D after B6 (P < 0.05). Serum cholesterol and triglyceride levels did not change. Disorders of amino acid metabolism in D were studied by measuring fasting plasma amino acid levels and metabolic clearance rates of essential amino acids. Metabolic clearance rate was significantly lower in D (P 6. Fasting plasma levels of valine, leucine, tryptophan, serine, glutamine, alanine, and tyrosine were significantly lower in D compared to C. After pyridoxine supplementation, plasma valine, leucine, serine, glutamine, and alanine increased to C levels, while tryptophan and tyrosine did not change. Changes in fasting plasma amino acid and serum high-density lipoprotein levels after correction of the biochemical deficiency of vitamin B6 in D indicates that vitamin B6 deficiency may contribute significantly to the pathogenesis of the abnormal amino acid and lipid metabolism in D.